Results 231 to 240 of about 278,156 (310)
RETRACTED: Sobeh et al. A Polyphenol-Rich Fraction from <i>Eugenia uniflora</i> Exhibits Antioxidant and Hepatoprotective Activities In Vivo. <i>Pharmaceuticals</i> 2020, <i>13</i>, 84. [PDF]
Sobeh M +6 more
europepmc +1 more source
Human ABCE1 cannot functionally replace its yeast ortholog. Yeast–human chimera analysis identified NBD1 as a major interspecies barrier. Genetic screening yielded hABCE1 revertants that rescue yeast viability but fail to suppress aberrant translation reinitiation in the 3′ UTR.
Eriko Nakata +3 more
wiley +1 more source
Ethical Considerations in Personal Health Large Language Models. [PDF]
Liu J, Liu S.
europepmc +1 more source
MARK4 enhances stress granule formation under oxidative stress and increases tau accumulation
MARK4 (red dots) localizes to stress granules (orange dots) and promotes their formation under oxidative stress by modulating TIA1 (blue dots). MARK4 and TIA1 synergistically increase tau (purple) accumulation, and the reduction of the TIA1 ortholog suppresses neurodegeneration in a fly model.
Sho Nakajima +8 more
wiley +1 more source
Corrigendum to "Rap1 organizes lymphocyte front-back polarity via RhoA signaling and talin1" [iScience, Volume 26, Issue 8 (2023) 107292]. [PDF]
Ueda Y +8 more
europepmc +1 more source
Aging Is a Key Driver for Adult Acute Myeloid Leukemia
Acute myeloid leukemia (AML) is a classical age‐related hematologic malignancy, and a key driver of AML is aging, which profoundly regulates intrinsic factors such as genomic instability, epigenetic reprogramming, and metabolic dysregulation, and alters bone marrow microenvironment.
Rong Yin, Haojian Zhang
wiley +1 more source
Evolutionary game research on multi-agent collaboration within financial reporting internal control. [PDF]
Zhai X, Kou C.
europepmc +1 more source
Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance
NPM1 mutations drive acute myeloid leukemia by acting as neomorphic transcriptional regulators that cooperate with Menin–MLL and XPO1 to sustain HOX/MEIS1 expression and block differentiation. Targeting these mutant‐specific transcriptional dependencies provides a rational therapeutic strategy for NPM1‐mutated AML.
Yanan Jiang +3 more
wiley +1 more source

